Our objectives are to find out the relationship between the ouabain-resistant Na-Li exchange and the ouabain-resistant net Na extrusion systems present in human red cells. Both transport systems seem to be under genetic control. The exchange is enhanced while the net Na transport is reduced in red cells of patients with essential hypertension. We will investigate the hypothesis that a genetically defective co-transport system might be accompanied by an increase in the number of transport units exchanged Na for Na in a 1:1 fashion. A second hypothesis to be investigated is the regulatory role of humoral factors in the Na-Li countertransport. These studies may allow the understanding of the pathogenic or regulatory role of the ouabain-resistant Na and K transport in essential hypertension, a disease which affects 10% of the human population.